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Neurological Complications Resulting from Non-Oral Occupational Methanol Poisoning
Choi, Ji-Hyun,Lee, Seung Keun,Gil, Young-Eun,Ryu, Jia,Jung-Choi, Kyunghee,Kim, Hyunjoo,Choi, Jun Young,Park, Sun Ah,Lee, Hyang Woon,Yun, Ji Young The Korean Academy of Medical Sciences 2017 JOURNAL OF KOREAN MEDICAL SCIENCE Vol.32 No.2
<P>Methanol poisoning results in neurological complications including visual disturbances, bilateral putaminal hemorrhagic necrosis, parkinsonism, cerebral edema, coma, or seizures. Almost all reported cases of methanol poisoning are caused by oral ingestion of methanol. However, recently there was an outbreak of methanol poisoning via non-oral exposure that resulted in severe neurological complications to a few workers at industrial sites in Korea. We present 3 patients who had severe neurological complications resulting from non-oral occupational methanol poisoning. Even though initial metabolic acidosis and mental changes were improved with hemodialysis, all of the 3 patients presented optic atrophy and ataxia or parkinsonism as neurological complications resulting from methanol poisoning. In order to manage it adequately, as well as to prevent it, physicians should recognize that methanol poisoning by non-oral exposure can cause neurologic complications.</P>
Jia, Yuefa,Liu, Jia,Cha, Sangwon,Choi, Soobin,Park, Yun Chang,Liu, Chunli THE KOREAN SOCIETY OF INDUSTRIAL AND ENGINEERING 2017 JOURNAL OF INDUSTRIAL AND ENGINEERING CHEMISTRY -S Vol.47 No.-
<P><B>Abstract</B></P> <P>Magnetically recyclable Au-TiO<SUB>2</SUB>/nanocube ZnFe<SUB>2</SUB>O<SUB>4</SUB> (Au-TiO<SUB>2</SUB>/NC ZFO) composite photocatalysts have been successfully prepared by a hydrothermal method. It was revealed that Au-TiO<SUB>2</SUB>/NC ZFO composite with 25% mass percentage of Au-TiO<SUB>2</SUB> exhibited a significantly enhanced photocatalytic efficiency toward chlortetracycline (CTC) degradation as compared to the binary TiO<SUB>2</SUB>/NC ZFO composite. The enhanced performance can be attributed to the addition of Au nanoparticles, which act as electron traps aiding the electron-hole separation and increasing the light absorption through the surface plasmon resonance effect. The synthesized catalyst showed good stability after three cycles and could be easily separated by a magnet and reused.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A new type ternary Au-TiO<SUB>2</SUB>/nanocube ZnFe<SUB>2</SUB>O<SUB>4</SUB>. </LI> <LI> The Au-TiO<SUB>2</SUB>/nanocube ZnFe<SUB>2</SUB>O<SUB>4</SUB> shows superior photocatalytic activity. </LI> <LI> The chlortetracycline can be removed by Au-TiO<SUB>2</SUB>/nanocube ZnFe<SUB>2</SUB>O<SUB>4</SUB>. </LI> <LI> Cycle degradation tests show the catalyst was highly active, stable and recoverable. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>Magnetically separable Au-TiO<SUB>2</SUB>/nanocube ZnFe<SUB>2</SUB>O<SUB>4</SUB> composite exhibit an outstanding photocatalytic activity in degradation of chlortetracycline (CTC) under visible light irradiation.</P> <P>[DISPLAY OMISSION]</P>
Jia, Lina,Lee, Hun Seok,Wu, Chun Fu,Kundu, Juthika,Park, Sang Gyu,Kim, Ryong Nam,Wang, Li-Hui,Erkin, Ö,zgü,r Cem,Choi, Jong-Sun,Chae, Seoung Wan,Yang, Ho Bin,Choi, Yoon-La,Shin, Young Kee American Association for Cancer Research 2014 Molecular Cancer Research Vol.12 No.12
<P>SMAD4 has been suggested to inhibit the activity of the WNT/β-catenin signaling pathway in cancer. However, the mechanism by which SMAD4 antagonizes WNT/β-catenin signaling in cancer remains largely unknown. Aurora A kinase (AURKA), which is frequently overexpressed in cancer, increases the transcriptional activity of β-catenin/T-cell factor (TCF) complex by stabilizing β-catenin through the inhibition of GSK-3β. Here, SMAD4 modulated AURKA in a TGFβ-independent manner. Overexpression of SMAD4 significantly suppressed AURKA function, including colony formation, migration, and invasion of cell lines. In addition, SMAD4 bound to AURKA induced degradation of AURKA by the proteasome. A luciferase activity assay revealed that the transcriptional activity of the β-catenin/TCF complex was elevated by AURKA, but decreased by SMAD4 overexpression. Moreover, target gene analysis showed that SMAD4 abrogated the AURKA-mediated increase of β-catenin target genes. However, this inhibitory effect of SMAD4 was abolished by overexpression of AURKA or silencing of AURKA in SMAD4-overexpressed cells. Meanwhile, the SMAD4-mediated repression of AURKA and β-catenin was independent of TGFβ signaling because blockage of TGFβR1 or restoration of TGFβ signaling did not prevent suppression of AURKA and β-catenin signaling by SMAD4. These results indicate that the tumor-suppressive function of SMAD4 is mediated by downregulation of β-catenin transcriptional activity via AURKA degradation in a TGFβ-independent manner.</P><P><B>Implications:</B> SMAD4 interacts with AURKA and antagonizes its tumor-promoting potential, thus demonstrating a novel mechanism of tumor suppression. <I>Mol Cancer Res; 12(12); 1779–95. ©2014 AACR</I>.</P>